[Screening and rapid tests in adrenal gland insufficiency].
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To assess the effects of d-norgestrel on pituitary-adrenal-ovarian function, basal levels and responses to metyrapone of urinary 17-ketogenic steroids (17-KGS) and 17-ketosteroids (17-KS), plasma cortisol (F), plasma delta4-androstenedione (A), plasma testosterone (T), plasma estrone (E1) and estradiol (E2), plasma and urinary LH and FSH were determined in 10 normal women before and while taking d-norgestrel 1 mg/day. Cortisol secretion rate (CSR) and binding capacities of cortisol binding globulin (CBG) and testosterone-estradiol binding globulin (TeBG) were also measured. Norgestrel did not significantly alter 17-KGS, 17-KS, F, LH, FSH, CSR, or the 17-KGS and 17-KS responses to metyrapone. Norgestrel reduced TeBG binding capacity but not CBG binding capacity. Norgestrel competitively inhibited the binding of dihydrotestosterone to TeBG under in vitro conditions. Levels of T, E2, and E1 were reduced by norgestrel. All measured hormone levels except FSH were increased following metyrapone prior to norgestrel administration. Norgestrel completely blocked the metyrapone-induced increases in LH and E2 and markedly reduced the E1 increase. Metyrapone reduced E2 during norgestrel treatment.
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The systemic effect of 6alpha,9-difluor-11beta-hydroxy-16alpha-methyl-21-valeryloxy-1,4-pregnadiene-3,20-dione (diflucortolone valerate, Nerisona) 0.1% as an ointment and fatty ointment was investigated in two studies. The parameters used were the plasma 11-OHCS values and the urinary 17-OHCS and 17-KS values, respectively. Suppression of the plasma cortisol values was observed after topical application of both diflucortolone valerate and betamethasone-17-valerate to healthy subjects under extreme conditions of whole-body occlusion. However, it was still possible to stimulate the adrenal cortex with ACTH. No reduction of the 17-OHCS of 17-KS values in the 24-h urine was observed during open, large-surface treatment of patients with skin diseases.
The functional state of the cortical and medullar layers of the adrenal glands was studied in 127 patients with primary arterial hypotension (109 females and 18 males, aged 17 to 48 years). As shown by daily urine excretion, hypotonic patients had a decreased basal activity of the glucocorticoid and androgenic function of the adrenal cortex in comparison with those in normal individuals. The potential of the adrenal cortex was preserved in these patients within sufficient limits. The adrenocorticotrophic function of the anterior lobe of the pituitary gland was found to decrease. Against the background of a reduction of the total excretion of all fractions a relative delay was noted in the process of glucocorticoids transformation into their precursors, as well as a relative predominance of glucocorticoids over mineralcorticoids, the content of desoxycorticosterone being reduced especially low. The content of adrenalin, noradrenaline and dophamine was below the normal level, the decrease being statistically significant. At the same time the excretion of DOPA was normal, on the average, the whole group of patients. The changes in the daily urine excretion of catecholamines and DOPA, as well as in their ratio indicate that the activity of both links of the sympathodrenal system is reduced in primary arterial hypotension.
The authors report a case of Steinert's disease in a woman and discuss the endocrine profile of this disease after giving an account of the criteria of diagnosis. Disorders of gonad function are mild in women, primary testicular atrophy is very frequent in man with reduction in 17-ketosteroids and testosterone. Thyroid function was normal but, in a few cases, a low fixation curve was found (our case) corrected by TSH stimulation. The frequency of cataract emphasizes the interest of this sign for detection. Diabetes, associated with hyperinsulinism, seemed more frequent than in a population without Steinert's disease. The pathogenesis of these endocrine disorders appears secondary and is ill explained if one considers it as a single disease. Better knowledge, no doubt linked to progress in biochemistry of normal and myopathic muscle, will help to explain the pathogenesis.
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The results of biochemical examinations of the hormonal function of the adrenal cortex in 22 patients with Parkinson's disease are presented as seen prior and following stereotaxic operations on the ventro-lateral nucleus of the thalamus. It was found that parkinsonics have a decreased androgenic, glucocorticoid and mineralocorticoid function of the adrenal cortex. Long history and growing severity of the disease manifest themselves in a distinct inhibition of the adrenal cortex function. The importance of the changes in the functional state of the hypothalamo-hypophyseal system in the revealed disorders in the hormonal activity is emphasized. Along with a beneficial clinical effect surgery brings about an improvement of the functional state of the adrenal cortex.
In the United States the etiology of most cases of adrenal gland atrophy or destruction is unknown. Autoimmune processes may be responsible. With rare exceptions, all three zones of the adrenal cortex are destroyed and there is reduced glucocorticoid, mineralocorticoid and androgen secretion. Although the deficiency of glucocorticoid is probably the most severe threat to life, treatment is available to correct all the deficiencies. Patient education and preparedness can prevent serious complications.
Ascorbic acid administered for 18-20 days (daily by 100 mg per 1 kg of weight per os) causes redistribution of certain fractions of 17-OCS excreted with urine (a decrease in the content of free F and F/E ratio, an increase in the content of THF, THE and THS, a more frequent appearance of substances). In the blood plasm and adrenals concentration of 11-OCS rises. When determining the available functional reserves of the adrenal cortex under these conditions, an increase in the content of F, E and S unchanged forms is observed in response to ACTH administration as distinct from the initial state. The rise in concentration of 11-OCS in the adrenals and blood plasm is less pronounced than in the control. A conclusion is drawn that ascorbic acid affects metabolism of glucocorticoids and changes the reaction of the adrenaocortical system on the action of ACTH.
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In the light of seven cases of adrenal hypercorticalism associated with tumoral secretion of ACTH, the syndrome of inappropriate ACTH secretion is reviewed. This entity, which is related primarily to anaplastic bronchial carcinoma is characterized by paucity of clinical signs of hypercorticalism, rapidity of evolution and typical biological modifications. Other important criteria are hypokalemic alkalosis, high plasma levels of ACTH and 17-OHCS and failure of dexamethasome to suppress endogenous steroid secretion. However, the diagnosis can be proven only by extraction of a significant quantity of tumoral ACTH.
In administration to quinea pigs of ethyl-p-chlorophenoxyisobutyrate daily in a dose of 0.2 g/kg per os for 15-26 days decreased the 17-OHCS concentration in the peripheral blood plasma. A fall of the urinary excretion of individual 17-OHCS occurred chiefly at the expense of free unchanged cortisol, tetrahydrocortisol and tetrahydro-11-desoxycortisol. The zona fasciculate displays the abundance of the sudanophilic material. A test with ACTH demonstrated that the present functional reserves of the adrenal cortex failed to change under the effect of the preparation. The content of NEFA decreased in the blood serum; as to cholesterol level - it reamined unchanged. Possible mechanisms of the action of the preparation and prospects of its use for the treatment of hypercorticism are discussed.
A study was made of 77 patients with adiposity and a group of healthy persons with normal weight. Patients with adiposity had a significant increase of blood plasma aldosterone level; of decisive role in the formation of secondary hyperaldosteronism was played by the elevation of blood renin level. Apparently activation of the renin-angiotensin system and the associated intensification of mineralocorticoid function of the adrenal glands served as one of the causes of development of arterial hypertension in persons with excessive weight. In adiposity there proved to be an increased rate of cortizol secretion and of 17-OCS excretion with the urine; as to the blood plasma cortizol concentration, it failed to show any significant difference from the normal. Apparently stable blood cortizol level in the patients with adiposity was maintained as a result of intensified ACTH secretion; in these patients reserve possibilities of the adrenocorticosteroid function of the hypophysis were diminished.
The authors present the results of study of the basic blood testosterone level and of the 17-ketosteroid urinary excretion under conditions of a test with dexamethasone and choriongonin. The results obtained were compared with the results of analogous examination of a group of patients with the virile form of the Stein-Loewenthal's syndrome. Blood testosterone level served as a significant criterion in the diagnosis of virilizing tumours of the testes. Besides, a study was made of the remote results of sparing surgical tactics in the treatment of virilizing tumours of the testes lasting up to 13 years in 37 patients. Favourable results pointed to the benign course of these tumours and justified conservative therapy.
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The circadian rhythm of plasma cortisol and urinary 17-hydroxy-corticosteroids has been studied in 6 normal volunteers both in basal conditions and after the administration of a single dose of 30 mg of a banthine derivative (the beta methyl-beta-isopropylaminoethyl ester bromide of xantene-9-carbonic acid, "Pervagal") given orally once a day at different hours (midnight, 4 AM, 8 AM, noon, 4 PM, 8 PM). The vagolytic drug inhibits the cortisol secretion only when administered at 4 PM, 8 PM or midnight, whereas it is ineffective when given at different hours. If don't exist circadian variations of the bio-availability of the drug employed, our results suggest that also in human beings as well as in experimental animals, the cholinergic mechanisms are effective, over all if not exclusively, in starting the circadian activation of the hypothalamo-pituitary-adrenal system.